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首页> 外文期刊>World Journal of Gastroenterology >Detection of point mutation in K-ras oncogene at codon 12 in pancreatic diseases
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Detection of point mutation in K-ras oncogene at codon 12 in pancreatic diseases

机译：胰腺疾病第12位密码子K-ras癌基因点突变的检测

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AIM: To investigate frequency and clinical significance of K-ras mutations in pancreatic diseases and to identify its diagnostic values in pancreatic carcinoma. METHODS: 117 ductal lesions were identified in the available sections from pancreatic resection specimens of pancreatic ductal adenocarcinoma, comprising 24 pancreatic ductal adenocarcinoma, 19 peritumoral ductal atypical hyperplasia, 58 peritumoral ductal hyperplasia and 19 normal duct at the tumor free resection margin. 24 ductal lesions were got from 24 chronic pancreatitis. DNA was extracted. Codon 12 K-ras mutations were examined using the two-step polymerase chain reaction (PCR) combined with restriction enzyme digestion, followed by nonradioisotopic single-strand conformation polymorphism (SSCP) analysis and by means of automated DNA sequencing. RESULTS: K-ras mutation rate of the pancreatic carcinoma was 79%(19/24) which was significantly higher than that in the chronic pancreatitis 33%(8/24) (P<0.01). It was also found that K-ras mutation rate was progressively increased from normal duct at the tumor free resection margin, peritumoral ductal hyperplasia, peritumoral ductal atypical hyperplasia to pancreatic ductal adenocarcinoma. The mutation pattern of K-ras 12 codon of chronic pancreatitis was GGT→GAT, GGT and CGT, which is identical to that in pancreatic carcinoma. CONCLUSION: K-ras mutation may play a role in the malignant transformation of pancreatic ductal cell. K-ras mutation was not specific enough to diagnose pancreatic carcinoma.
机译：目的：探讨胰腺疾病中K-ras基因突变的频率和临床意义，并确定其在胰腺癌中的诊断价值。方法：从胰管腺癌胰腺切除标本的可用切片中鉴定出117个导管病变，包括24个胰腺导管腺癌，19个肿瘤周围导管非典型增生，58个肿瘤周围导管增生和19个正常导管在无肿瘤切除边缘。 24例慢性胰腺炎共得到24例导管病变。提取DNA。使用两步聚合酶链反应（PCR）结合限制性内切酶消化，然后进行非放射性同位素单链构象多态性（SSCP）分析并通过自动DNA测序，检查密码子12 K-ras突变。结果：胰腺癌的K-ras突变率为79％（19/24），明显高于慢性胰腺炎的33％（8/24）（P <0.01）。还发现，K-ras突变率从无肿瘤切除边缘的正常导管，肿瘤周围导管增生，肿瘤周围导管非典型增生到胰腺导管腺癌逐渐增加。慢性胰腺炎的K-ras 12密码子突变模式为GGT→GAT，GGT和CGT，与胰腺癌相同。结论：K-ras突变可能与胰腺导管细胞恶性转化有关。 K-ras突变不足以诊断胰腺癌。

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